Acquired immune deficiency syndrome and its related diseases was first recognized in about 1971, but it was only recently that the etiologic cause of the disease was isolated and identified as a human retrovirus named human immunodeficiency virus (HIV). HIV includes human T-lymphotropic virus type III (HTLV-III), lymphadenopathy-associated virus (LAV), and AIDS-associated retrovirus (ARV).
AIDS is generally recognized as epidemic in several areas of the world, including the United States. At present, the groups at highest risk of infection with HIV include homosexual and bisexual men and abusers of injected drugs. It is also known, however, that AIDS is transmitted heterosexually.
HIV acts by crippling the body's immune system. Particularly, HIV selectively attacks T4 cells, a subpopulation of helper/inducer lymphocytes which constituted part of the immune system. Infection with HIV results in both a reduction in the number and a change in function of the targeted T4 lymphocytes with eventual collapse of the immune system. Thus, the disease manifests itself as severe immunosuppression typically resulting in devastating opportunistic infections and neoplasias.
Present methods of treating AIDS are limited and largely ineffective. There is no known cure for AIDS, and in fact, effective treatment of a retroviral infection in man is unprecedented. Known therapies are generally limited to regimens designed to treat the secondary infections and neoplasias associated with AIDS. At present, AIDS has been treated with immunomodulators, such as cimetidine and interleukin-2, indomethacin, an antiinflammatory and prostaglandin inhibitor, and azidithymidine (AZT). None of the known therapies has been totally effective.
Recently, the subregion of the HIV external glycoprotein molecule, gp120, responsible for binding to brain membrane and human T cells has been identified as an octapeptide referred to as peptide T (Ala-Ser-Thr-Thr-Thr-Asn-Tyr-Thr). It has also been reported that peptide T and certain analogs thereof block the binding of HIV to T4 cells. C. B. Pert et al, Proc. Natl. Acad. Sci., Vol. 83, pp. 9254-9258, December 1986. Further, a correlation between the binding of peptide T to the T4 (CD4) surface molecule and the ability of the peptide to promote monocyte migration has also been reported. M. R. Ruff et al., FEBS Letters, Vol. 211, Number 1, pp. 17-22, January 1987.
A homology has been reported between peptide T and segments of other proteins, in particular, ribonuclease (segment 19-26), vasoactive intestinal peptide and a pentapeptide isolated from HTLV-III and LAV. M. R. Pincus et al., Biochem. Biophys. Res. Comm., Vol. 143, No. 1, pp. 248-251, 1987.
The present invention provides novel synthetic penta, hexa, hepta and octapeptides useful for the treatment of AIDS and a method for treating AIDS by administering the peptides of the invention.